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Friday, February 17, 2017

Hormone Prostaglandins and hepatocellular carcinoma cells

Kyle J. Norton(Scholar and Master of Nutrients, all right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.                     

                      Hormone Prostaglandins

Prostaglandins, are a group of lipid mediators, found and isolated from human semen in the 1930s by Ulf von Euler of Sweden, responsible for inflammation features, such as swelling, pain, stiffness, redness and warmth. The hormones are produced by almost all nucleated cells and synthesized in the cell from the essential fatty acids (EFAs), include prostacyclin I2 (PGI2), prostaglandin E2(PGE2), and prostaglandin F2α (PGF2α)

     Hormone Prostaglandins & hepatocellular carcinoma cells


Prostaglandin E2 has been implicated in cell growth and metastasis in many types of cancers. According to the study by Nanjing Medical University, showed that PGE2 treatment significantly increased the cell adhesion, migration, and invasion in hepatocellular carcinoma (HCC) cells. In addition, the effects of PGE2 were found to be associated with focal adhesion kinase (FAK). PGE2 treatment increased the phosphorylation and synthesis of FAK in a dose-dependent manner. RNA interference targeting FAK suppressed PGE2-mediated cell adhesion and migration. Furthermore, the downstream proteins of FAK, paxillin and Erk2, were also activated by PGE2. PGE2 treatment increased the phosphorylation and synthesis of paxillin in a dose-dependent manner. PGE2 treatment also induced the phosphorylation of Erk2(8).

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Sources
(8) http://www.ncbi.nlm.nih.gov/pubmed/19082453

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